Perfusion of Intrapulmonary Arteriovenous Anastomoses Is Not Related to VO in Hypoxia and Is Unchanged by Oral Sildenafil.

Perfusion of intrapulmonary arteriovenous anastomoses (IPAVA) is increased during exercise and in hypoxia and is associated with variations in oxygen saturation (SO), resulting in blood bypassing the pulmonary microcirculation. Sildenafil is a pulmonary vasodilator that improves SO and endurance performance in hypoxia. The purpose of this study was to determine if 50 mg sildenafil would reduce IPAVA perfusion (Q) and if the decrement in maximal exercise capacity (VO) in hypoxia is related to Q. We hypothesized that during progressive levels of hypoxia at rest (FO = 0.21, 0.14, 0.12), sildenafil would increase SO and reduce bubble score (estimate of Q) compared to placebo, and that the decrement in VO in hypoxia would be positively correlated with bubble score at rest in hypoxia. Fourteen endurance-trained men performed a graded maximal exercise test at sea level and at a simulated altitude of 3000 m, followed by two experimental visits where, after randomly ingesting sildenafil or placebo, they underwent agitated saline contrast echocardiography during progressive levels of hypoxia at rest. All participants experienced a decrement in power output in hypoxia that ranged from 9% to 19% lower than sea level values. Compared to normoxia, bubble score increased significantly in hypoxia ( < 0.001) with no effect of sildenafil ( = 0.580). There was a negative correlation between SO and bubble score ( < 0.001). The decrement in peak power output at VO in hypoxia was unrelated to IPAVA perfusion in resting hypoxia ( = 0.32). Several participants demonstrated Q greater than zero in room air, indicating that arterial hypoxemia may not be the sole mechanism for Q. These results indicate that the VO decrement caused by hypoxia is not related to Q and that sildenafil does not improve VO in hypoxia through modulation of Q.